Institutional Repository of Key Laboratory of Ion Beam Bioengineering, Hefei Institutes of Physical Science, Chinese Academy of Sciences, Hefei, Anhui 230031, People's Republic of China
LncRNA MT1DP Aggravates Cadmium-Induced Oxidative Stress by Repressing the Function of Nrf2 and is Dependent on Interaction with miR-365 | |
Gao, Ming1,2; Li, Changying3; Xu, Ming1,2; Liu, Yun1,4; Cong, Min3; Liu, Sijin1,2 | |
2018-07-01 | |
发表期刊 | ADVANCED SCIENCE |
ISSN | 2198-3844 |
通讯作者 | Liu, Sijin(sjliu@rcees.ac.cn) |
摘要 | Although cadmium (Cd)-induced hepatoxicity is well established, pronounced knowledge gaps remain existed regarding the inherent cellular signaling that dictates Cd toxicity. Specifically, the molecular basis for determining the equilibrium between prosurvival and proapoptotic signaling remains poorly understood. Thus, it is recently revealed that long non-coding RNA (lncRNA) MT1DP, a pseudogene in the metallothionein (MT) family, promoted Cd-induced cell death through activating the RhoC-CCN1/2-AKT pathway and modulating MT1H induction. Here, first the dependency of MT1DP induction on MTF1, an important transcriptional factor in driving the mRNA expression of MT1 members is defined. Additionally, a bridge molecule between MT1DP and nuclear factor erythroid 2-related factor 2 (Nrf2) is established: miR-365. Mechanistically, MT1DP induction under Cd stress decreases the nuclear factor erythroid 2-related factor 2 (Nrf2) level to evoke oxidative stress through the elevation of miR-365, which acted to repress the Nrf2 level via direct binding to its 3'UTR. In contrast to the competing endogenous RNA (ceRNA) mechanism, a new mechanism is proposed: MT1DP elevated the miR-365 level though stabilizing its RNA via direct binding. Collectively, the combined data demonstrate a crucial role of MT1DP in reducing the Nrf2-mediated protection of cells, and this is dependent on the interplay with miR-365. Hence, the study further expands the knowledge of inducible endogenous lncRNA in modulating oxidative stress. |
关键词 | cadmium long non-coding RNA (lncRNA) miR-365 MT1DP Nrf2 oxidative stress |
DOI | 10.1002/advs.201800087 |
关键词[WOS] | LONG NONCODING RNA ; ERYTHROID-CELLS ; FACTOR-I ; TOXICITY ; LIVER ; GENE ; MECHANISMS ; EXPRESSION ; PATHWAYS ; EXPOSURE |
收录类别 | SCI |
语种 | 英语 |
资助项目 | Strategic Priority Research Program of the Chinese Academy of Sciences[XDB14000000] ; National Natural Science Foundation of China[21507154] ; National Natural Science Foundation of China[21425731] ; National Natural Science Foundation of China[21637004] ; National Natural Science Foundation of China[81570542] ; national 973 program[2014CB932000] ; Strategic Priority Research Program of the Chinese Academy of Sciences[XDB14000000] ; National Natural Science Foundation of China[21507154] ; National Natural Science Foundation of China[21425731] ; National Natural Science Foundation of China[21637004] ; National Natural Science Foundation of China[81570542] ; national 973 program[2014CB932000] |
项目资助者 | Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; Strategic Priority Research Program of the Chinese Academy of Sciences ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; National Natural Science Foundation of China ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program ; national 973 program |
WOS研究方向 | Chemistry ; Science & Technology - Other Topics ; Materials Science |
WOS类目 | Chemistry, Multidisciplinary ; Nanoscience & Nanotechnology ; Materials Science, Multidisciplinary |
WOS记录号 | WOS:000439842100017 |
出版者 | WILEY |
引用统计 | |
文献类型 | 期刊论文 |
条目标识符 | http://ir.hfcas.ac.cn:8080/handle/334002/37691 |
专题 | 技术生物与农业工程研究所 |
通讯作者 | Liu, Sijin |
作者单位 | 1.Chinese Acad Sci, Res Ctr Ecoenvironm Sci, State Key Lab Environm Chem & Ecotoxicol, Beijing 100085, Peoples R China 2.Univ Chinese Acad Sci, Coll Resources & Environm, Beijing 100049, Peoples R China 3.Capital Med Univ, Beijing Friendship Hosp, Liver Res Ctr, Beijing 100050, Peoples R China 4.Chinese Acad Sci & Anhui Prov, Hefei Inst Phys Sci, Key Lab Ion Beam Bioengn, Hefei 230031, Anhui, Peoples R China |
推荐引用方式 GB/T 7714 | Gao, Ming,Li, Changying,Xu, Ming,et al. LncRNA MT1DP Aggravates Cadmium-Induced Oxidative Stress by Repressing the Function of Nrf2 and is Dependent on Interaction with miR-365[J]. ADVANCED SCIENCE,2018,5(7):9. |
APA | Gao, Ming,Li, Changying,Xu, Ming,Liu, Yun,Cong, Min,&Liu, Sijin.(2018).LncRNA MT1DP Aggravates Cadmium-Induced Oxidative Stress by Repressing the Function of Nrf2 and is Dependent on Interaction with miR-365.ADVANCED SCIENCE,5(7),9. |
MLA | Gao, Ming,et al."LncRNA MT1DP Aggravates Cadmium-Induced Oxidative Stress by Repressing the Function of Nrf2 and is Dependent on Interaction with miR-365".ADVANCED SCIENCE 5.7(2018):9. |
条目包含的文件 | 条目无相关文件。 |
除非特别说明,本系统中所有内容都受版权保护,并保留所有权利。
修改评论